Volume status is a critical consideration when treating ill patients and arguably the most debated modifiable parameter. Patients who are felt to be hypovolemic, or “dry,” are usually given volume resuscitation in hopes of improving cardiac output. Patients who are felt to be hypervolemic, or “wet,” typically undergo diuresis, either from medication or dialysis machines. On average, fifty percent (50%) of all fluid boluses in Intensive Care Units do not improve cardiac output. In these patients, the additional volume does not benefit the patient. Rather, the extraneous volume may actually hurt the patient. Extraneous volume may reduce renal perfusion, inhibit wound healing, inhibit gut absorption, and/or compromise pulmonary function. In some cases, the additional fluid may actually worsen cardiac output, the precise parameter the fluid bolus was attempting to improve.
Thus, there is a need to improve the ability to determine volume status and subsequently volume responsiveness in patients.
There is growing data over the last decade suggesting the current ‘gold standard’ of volume status is suboptimal. The current management of determining volume status includes measurement of the central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP, or wedge pressure) as indicators of volume status. Newer ‘dynamic’ techniques, such as pulse pressure variation (the change in systemic blood pressure with respiration), have repeatedly outperformed the older, ‘static’ methods. However, the newer dynamic techniques have patient requirements that limit more widespread adoption of these methods. Pulse pressure variation is limited, amongst other limitations, to patients who are intubated, ventilated at high tidal volumes, and not spontaneously breathing. Furthermore, determining responses to these maneuvers are cumbersome and not easily accessible.
Described herein are various systems and methods aimed to measure and/or optimize volume status in ill patients.
Recently, there has been a growing emphasis on minimally invasive monitors of hemodynamic parameters. From external echocardiograms to complex interpretation of arterial waveforms, the industry has largely moved away from inserting long catheters into the body. However, this move is predicated on the lack of therapeutic benefit. As long as these monitors are purely diagnostic, it is understandable to minimize invasive procedures that place patients at risk. However, a temporary device that optimizes both heart rate and intra-cardiac filling pressures has the potential to improve cardiac output while optimizing pulmonary function. Such a device may benefit the patient and make an invasive procedure to insert the device both practical and beneficial.
The principle underlying CVP or PAOP-based fluid management presumes in a setting of low CVP or PCWP is that administering fluid boluses (and thereby increasing these parameters) will improve cardiac output, and this will have beneficial effects on tissue perfusion and lead to improved clinical outcome. Conversely, in the setting of an elevated CVP or PCWP, administering fluid boluses will fail to improve cardiac output; instead, the extraneous fluid may result in volume overload, leading to impaired wound healing, gut absorption, pulmonary congestion, and worsening renal function. The usefulness of the traditional CVP or PAOP-based recordings have been challenged by various studies indicating changes in right atrial pressure or PCWP in response to fluid challenge do not translate to favorable changes in cardiac output.
The second primary analysis of the FACTT trial, along with the ESCAPE and PACMAN trials in patients with acute decompensated heart failure and a mixed group of medical and surgical patients, have failed to show that fluid management guided by a pulmonary artery catheter (PAC) improves outcomes compared to use of central venous pressure. Disappointingly, these parameters, often employed by critical care physicians, appear to be no better (and perhaps worse) in predicting volume responsiveness than flipping a coin.
Many studies demonstrate the utility of ‘dynamic measures’ for volume status determination, the concept being that, for a given patient, the optimal filling pressures are variable, i.e., some patients require very high filling pressures to maintain cardiac output while other patients maximize their cardiac output at very low pressures. Therefore, the concept of ‘dynamic’ methods includes measuring changes in surrogates to cardiac output in response to perturbations to the system.
For example, spontaneous and mechanical ventilation are accompanied by dynamic changes in intrathoracic and transpleural pressures. These dynamic changes also result in changes in stroke volume as well as changes in blood pressure. A number of studies demonstrate that pulse pressure variation predicts fluid responsiveness in critically ill or perioperative patients. In a prospective study of forty patients with septic shock who were mechanically ventilated, pulse pressure variation (defined as 100%×(maximal pulse pressure−minimal pulse pressure)/(mean pulse pressure)) of greater than 15% predicted an increase in cardiac index with an area under the receiver-operating characteristic (ROC) curve of 0.98; the areas under the curve (AUC) for CVP and PCWP were 0.51 and 0.40. PPVar of greater than 15% predicted fluid responsiveness with 94% sensitivity and 96% specificity.
Another smaller prospective observational study employed a PPVar threshold of 12% and found this predicted fluid responsiveness with 68% sensitivity and 100% specificity; CVP and PCWP were not predictive of fluid responsiveness. In a study of off-pump coronary artery bypass graft patients, pulse pressure variation greater than 13% predicted an increase in cardiac index with a fluid challenge with an AUC of 0.81. CVP and PCWP were not significant predictors of change in cardiac index. In a small study of high-risk surgical patients, intra-operative fluid management based on pulse pressure variation decreased ICU length of stay by six days and reduced postoperative complications.
There are other respiratory maneuvers that can be used to predict volume responsiveness. A small study of mechanically ventilated patients reported that pulse pressure variation after a fifteen second end-expiratory occlusion predicted an increase in cardiac index with 91% sensitivity and 100% specificity. This measure was significantly more predictive of fluid responsiveness than passive leg raising (sensitivity 48%, specificity 91%). In another recent study of spontaneously breathing patients, pulse pressure changes in response to a Valsalva maneuver predicted fluid responsiveness with a sensitivity and specificity of 91% and 95% respectively. These studies highlight the important of dynamic maneuvers to predict volume-responsiveness.
Stroke volume/cardiac output and heart rate are complicated parameters. Although cardiac output is the product of heart rate with stroke volume (HR×SV=CO), numerous studies have found the cardiac output to be remain strikingly unaltered with changes in heart rate. This has been found in resting and exercising dogs and resting and exercising humans. In these studies, the lower stroke volume during atrial pacing was accompanied by a lower CVP, indicating a redistribution of blood from the venous beds to the arterial and peripheral vascular beds. As venous return to the heart is not increased, the stroke volume will decrease with increasing heart rate implying an extrathoracic venous collapse. Previous studies have found that increasing atrial pacing significantly decreased central venous pressure (CVP), pulmonary artery wedge pressure (PCWP), and pulse pressure. Furthermore, volume status measurements are also complicated by irregular heart rates such as atrial fibrillation or frequent ectopic beats. In particular, dynamic variables are difficult to interpret since filling pressures are frequently changing.